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Pamela E. Knapp, Ph.D.
Professor
Ph.D., The Ohio State University, 1983
M.S., The Ohio State University, 1980
B.S., Cornell University, 1977
Postdoctoral training, Department of Anatomy and Cell Biology, Wayne State University
| Office Address: | | Department of Anatomy & Neurobiology | | | | Virginia
Commonwealth University Medical Campus | | | | Box 980709 | | | | Richmond, VA
23298-0709 | | Office
Phone: | | (804) 628-7570 | | FAX: | | (804) 828-9477 | | e-mail: | | peknapp@vcu.edu |
RESEARCH AND SCHOLARLY INTERESTS
Glial-neuronal interactions during development and disease processes; the neuropathogenesis of human immunodeficiency virus (HIV) and co-morbidity of substance abuse; myelination and dysmyelination; neuroimmune diseases; traumatic injuries of the CNS.
Normal development and function of the CNS requires that glial cells and neurons have normal interactions with one another. When either cell type is formed aberrantly or is targeted by a disease process, the function of the CNS is compromised. The underlying goal of the majority of projects in this laboratory is to understand how disease processes alter both intracellular and intercellular signaling events, resulting in neuropathological changes. While the lab has a long-standing interest in diseases of myelination and dysmyelination, our broader emphasis is on diseases that involve a significant neuroimmune component (e.g. HIV neuropathology, multiple sclerosis). We are also interested in altered glial signaling after traumatic injuries to the CNS. We also have had a long-term interest in the effect of endogenous and exogenous opiates on the function of glial cells, and are particularly interested in understanding how co-exposure to opiate drugs of abuse results in exacerbation of the neuropathology observed in HIV-infected patients. The laboratory uses state-of-the-art cellular and molecular strategies to model these questions both in vivo and in a tissue culture setting. Techniques include long term in vitro imaging studies, immunohistochemistry, in situ hybridization, ratiometric Ca++ imaging, quantitative immunoblotting, RNAi, PCR and unbiased stereology.
REPRESENTATIVE PUBLICATIONS
Hauser KF, El-Hage N, Steine-Martin A, Maragos WF, Nath A, Persidsky Y, Volsky DJ and Knapp PE (2007). HIV-1 neuropathogenesis: Glial mechanisms revealed through substance abuse. J. Neurochem. 100:567-586.
Zhao TY, Adams MH, Zou SP, El-Hage N, Hauser KF, and Knapp PE (2007). Silencing the PTEN gene is protective against neuronal death induced by HIV-1 Tat. J. Neurovirol.,13(2): 97-106.
Adjan VV, Hauser KF, Bakalkin G, Yakovleva T, Scheff SW and Knapp PE (2007). Caspase-3 activity is reduced after spinal cord injury in dynorphin deficient mice: Differential effects on glia and neurons. Neuroscience, Aug 14 [E-pub ahead of print].
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